Environment International, Vol. 16, pp. 353-361, 1990 0160-4120/90 $3.00 +.00 Printed in the U.S.A. All rights reserved. Copyright ©1990 Pergmnon Press plc

THE CONCEPT OF CRITICAL LEVEL AND IMPULSE NOISE

Donald Henderson, Fred Farzi, and Richard Daniolson Headng Research Laboratory, University of Buffalo, Department of Communicative Disorders and Sciences, Buffalo, NY 14260, USA

El 88-218 (Received 31 October 1988; accepted 5 January 1990)

Current noise standards are based on the assumption that predictable relationships exist between noise exposure (presented as either continuous or impulse noise) and hearing loss. These studies were conducted to expand on previous evidence that noise presentation above a critical level may disproportionately damage the cochlea. Chinchillas were exposed to noise conditions in which impact and impulse noise were presented at different peak amplitude levels and in different temporal patterns of presentation. While the amount of total acoustic energy was kept equal within each experiment, significant differences in hearing loss were seen with different peak amplitude levels of noise. Impact noise generated disproportionately greater hearing loss at amplitude levels above 119 dB peak SPL; impulse noise caused greater permanent threshold shift at 150 dB peak SPL than at 135 dB. The results suggest that a critical level of noise exposure may exist, partially dependent on the rate of noise presentation.

INTRODUCTION

The question of whether impulse noise is more damaging than continuous or intermit tent noise has both practical and theoretical implicat ions (Passchier-Vermeer 1983). From a practical perspec- tive, for equal amounts of energy, if impulse noise is more damaging than continuous noise, then public health standards should have special provisions for impulse noise. Therefore, a unified approach to noise standards, based on the Energy Principle, (Burns and Robinson 1969) would appear to be inappropriate. From a more basic perspective, impulse or impact noise seem to damage the cochlea in ways that are qualitatively different than the modes of damage as- sociated with continuous noise. Spoendlin and Brun (1973) observed structural damage in the cochlea when guinea pigs were exposed to noise over 120 dB. Spoendlin and Brun described the phenomenon of "critical level", reporting that exposure to noise above the critical level damaged the cochlea by mechanical

disruption (i.e., tearing, breaking, or edema). More recently, Hamernik et al. (1984a, 1984b) reported direct mechanical destruction of the Organ of Corti after exposure to impulse noise. Exposure to 100 impulses of 160 dB and an A- durations of 2 ms noise caused the chinchilla's organ of Corti to split be- tween the pillar cells and inner hair cells and rip from the basilar membrane for several millime- ters. The inner hair cells appeared normal, but their physiological integrity was doubtful. Hamernik et al. (1984a,1984b)report extreme examples of me- chanical trauma following exposure to impulse noise, but mechanical damage to the cochlea may occur for less intense exposures.

The audiometric consequences of mechanical dam- age in the cochlea are, at present, not known, but the occurrence of mechanical damage may be inferred from a dramatic increase in the amount of hearing loss secondary to a minor increase in the intensity of the exposure. For example, when the noise is contin-

353

354 D. Henderson et al.

uous or intermittent, there is a relatively orderly relation between the intensity of the exposure and the level of temporary threshold shift. Mills (1982) re- viewed studies from chinchillas, monkeys, and man and found that when a continuous noise is suffi- ciently intense to cause a temporary hearing loss, the magnitude of hearing loss increases 1.7 dB for each additional dB of noise. Henderson and Hamernik (1982) studied the relation between hearing loss and level of impact noise. When the level was increased from 99 to 119 dB, hearing loss grew at about 1.5 dB per dB of noise. However, above 114 dB hearing loss grew at much faster rate (approximately 5 dB of TTS for each dB increase in noise). The 119 dB level may be a transition zone, or a critical level, where the cochlea is damaged by direct mechanical destruction. The transition or critical level is probably not a fixed level, but as Price (1986) has shown, it is frequency dependent and is primarily determined by the acous- tic transformation of the external and middle ear. The auditory system is also sensitive to the temporal flow of acoustic stimulation. It is reasonable to expect that certain temporal patterns will be responsible for a marked reduction of energy transmission through the middle ear when the stapedius and tensor tympani muscles remain generally contracted due to the protective action of the acoustic reflex (Borg and Nilsson 1984). Other temporal patterns of exposure may allow some recovery between impulses thereby leading to less total hearing loss than would be ex- pected from the total energy of the exposure. The following two experiments explore the relation be- tween the critical level and the temporal pattern of exposure to either impact and impulse noise.

MATERIALS AND METHODS

Adult chinchillas were used as subjects (Experi- ment I: N--75; Experiment II: N=42). The animals were anesthetized (0.1 mg/kg Ketamine) and made monaural by the surgical destruction of the left coch- lea. A chronic bipolar electrode was then implanted in the region of the inferior colliculus using proce- dures outlined previously (Henderson et al. 1973). The animals were allowed to recover for several days prior to threshold testing.

Auditory evoked response (AER) was used to es- timate hearing thresholds. Three pre-exposure thresh- olds were measured at 0.5, 1, 2, 4, 8, and 16 kHz; the mean of three measurements was used to establish the pre-exposure thresholds for that animal. After the exposure, the animals were tested at post-exposure times of 0.25, 2, 8, 24, and 240 h, in order to estimate the amount of temporary threshold shift (TTS) and

the threshold recovery function. At 30 days post- exposure, thresholds were remeasured in order to estimate the amount of permanent threshold shift (PTS).

EXPERIMENT I: IMPACT NOISE

Animals were placed, singularly or in pairs, in separate, small (31 × 51 × 38 cm) cages located below a loudspeaker and were given free access to food and water. The animals were then exposed to electronically synthesized impact noise. The impact consisted of a burst of broadband noise, whose spectrum was shaped with an equalizer, so that it roughly approximated that of an impact generated by striking a steel plate with a hammer (Blakeslee 1978).

The electrical signal was generated by multiplying (Analog Devices AD534) the spectrally-shaped noise with the output from an exponential waveform genera- tor. The waveform generator controlled the repetition rate and envelope of the synthesized impact. The signal was amplified and transduced by a loudspeaker located above the animal's head. Fig. I shows the waveform and spectrum of the impact. The duration of the impact at a point 20 dB below the peak was 200 ms and the nominal rise time of the signal was 12 ms.

Table I reflects the exposure conditions for Exper- iment I. Two variables were systematically manipu- lated. (1) Experiments B, C and D were conducted to examine the effect of "rate of presentation", thus the impact was delivered at 1/s (B), 4/s (C), and 0.25/s (D). (2) Within each experiment, the effect of level was examined . The peak level was var ied be tween 107 and 143 dB, counterbalanced by total number of impacts (and exposure duration), to yield an equal amount of acoustic energy in all noise exposure con- ditions.

Results of Experiment I

After each of the exposures, hearing loss was mon- itored for 30 days at 0.5, 2, and 8 kHz at various times after the exposure. Fig. 2 shows the average tempo- rary threshold shift (TTS) immediately after the ex- posure for each of the levels at each of the three repetition rates, (i.e., 1/s (B), 4/s (C), and 0.25/s (D). The trend of the data is clear: as the peak level of the impulse is increased, the level of TTS increases at all test frequencies. The actual rate of increase in TTS with increased level was difficult to determine be- cause the audiometric test system limited TTS mea- surements above 70-80 dB. Thus, the level of TTS may even have been higher for some of the conditions (e.g., for peak levels of 131 dB and greater).

Critical level and impact noise 355

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the pressure time profile of the noise.

A perspective on the variability among subjects and groups is provided in Fig. 3. This figure shows the TTS for individual subjects, at each of the three test frequencies, for the seven levels of Experiment C. While the data overlap between groups, the 119 dB impulses may be at a transition point because of the extreme variability at this level (e.g., 15 dB TTS for one subject at 4 kHz to 85 dB TTS for two subjects at 2 and 8 kHz). By contrast, the higher levels (>119 dB) have relatively homogeneous results.

The experimental animals were retested 30 days after the exposure. The hearing loss at that time was defined as permanent threshold shift (PTS). The right side of Fig. 2 shows the average PTS for the

three experiments. There was a range in each of the three experiments where there was no significant PTS (107-125 for B and D, and 107-119 for C). Above these levels, however, there was a substantial in- crease in PTS. The results from individual subjects were quite consistent with the group averages. The right side of Fig. 3 shows the individual PTS for the animals in Experiment C, (rate = 4/s). Animals in the 107-119 dB groups recovered or had only minor amounts of PTS; in the 125 dB group, there was a large range from no shift to 60 dB PTS; above 125 dB, all animals developed severe PTS at all test frequencies. Thus, the transition level of 119 dB seen in the TTS data also appeared in the PTS results.

Level (dB Peak

Table 1. Exposure conditions for impact noise experiment.

Group B Group C Group D (Rate = I/s) (Rate = 4/s) (Rate = 0.25/s) Exposure Exposure Exposure Duration Duration Duration

107 20 d 5 d 80 d 113 5 d 30 h 20 d 119 30 d 7.5 h 5 d 125 7.5 d 1.8 h 30 h 131 1.8 h 0.47 h 7.5 h 137 0.48 h 0.12 h 1.8 h 143 0.12 h 1.8 min 0.47 h

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Critical level and impact noise 357

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The importance of the rate of presentation can be seen in Fig. 4. The top panels show the TTS and PTS data from the 113 dB exposures. When the rate of presentation was increased from 1 every 4 s (D) to 4 per s (C), TTS increased a minimum of 15 dB at 0.5 kHz to an average 29 dB at 2 and 8 kHz. However, all 113 dB groups recovered to essentially pre-expo- sure levels or to minimum amounts of PTS. The rate of presentation has more obvious influence for the data of the 125 dB exposures. The bottom two panels of Fig. 4 show that both TTS and PTS increased significantly as the rate of presentation was increased. These results were even more surprising, considering at 4/s the middle ear reflex could be expected to provide some measure of protection to the inner ear (by maintaining higher impedances to energy flow through the middle ear through sustained middle ear contraction).

The rate of presentation appears to be an impor- tant, but not particularly well-understood, variable. The greater losses seen with faster repetition rates may have been the result of the animals' susceptibil- ity to damage during a noise exposure. The biological effects of a single exposure may have caused a period of vulnerability in the cochlea, and if another im- pulse hit the cochlea during thts time, then the effects of that impulse would be even greater. Conversely, at the slower rates, the longer periods between im- pacts allowed for some recovery to occur. This period of vulnerability is seen in a number of quite different

experiments; i.e., Price (1976) showed that changes in the cochlear mierophonics of eats caused by bursts of noise, were directly dependent on the period of time that had elapsed since the last noise exposure. Also, Perkins (1975) showed that the amount of TTS, PTS, and hair cell loss was greatly enhanced when the rate of presentation of 50 impulses was increased from 1/min to 1/10 s. The next experiment examined the importance of rate or temporary pattern when the exposure consisted of impulses.

EXPERIMENT I1: IMPULSE NOISE

This experiment was designed to assess the impor- tance of the temporal pattern on acoustic energy in the production of noise-induced hearing loss.

Exposures took place in a non-reverberant envi- ronment. Animals were positioned in a tight restraint, in front of a high frequency driver. The "ringing" of the driver's diaphragm was controlled by digitally controlling the input voltages trailing the peak dis- placement of the diaphragm which produced the im- pulse. The time-amplitude history of the resultant acoustic impulse was thus maintained at 170 lxs A- duration, roughly approximating an impulse of a mil- itary rifle shot. Fig. 5 shows the six exposure condi- tions for Experiment II. In the first, impulses were presented at a rate of one impulse per second ("One per see" group). This group was a type of control for comparing results from the other conditions. The

358 D. Henderson et al.

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Critical level and impact noise 359

second condition, "Burst" had the same number of impulses, but they were presented at the rate of one per 50 ms. This condition was designed to maximize the potential contribution of the acoustic reflex. The third condition, the "Salvo" had pairs of impulses (separated by 50 ms.) repeated every second. This condition explored the possibility that an impulse of sufficient amplitude may cause a temporary state of vulnerability in the cochlea that renders the cochlea more prone to damage from ensuing impulses with minimal involvement of the acoustic reflex.

Each of these three temporal patterns were pre- sented at high (150 dB) and low (135 dB) levels. When the level was dropped from 150 to 135 dB, the number of exposures was increased from 100 to 3200. Thus, both the high- and low-level exposure had the same total energy. A comparison between the low- and high-level exposures may help discern the appro- priateness of the equal energy hypothesis (Atherlcy

1973), and may clarify the transition level or critical level for impulse noise.

Results of Experiment II

Hearing was monitored (at 0.5, 1, 2, 4, 8, and 16 kHz ) at 15 min after the exposure (TTS) and 30 days later (PTS). Fig.6 shows the median TTS and PTS among the groups exposed to impulse noise. The hearing loss produced by the 150 dB exposures is shown in the top two panels. The "Burst" condition developed substantially less TTS (p < 0.002) than the other two conditions, and no PTS. Presumably, the acoustic reflex was contracted for most of the expo- sure (total duration = 5.8 s) thereby reducing the effective level of the impulse reaching the cochlea. The "One per second" and "Salvo" groups have es- sentially the same TTS. However, the output of au- diometric equipment was limited and actual TTS levels might have been actually greater. The "Salvo" group

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360 D. Henderson et al.

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plitude levels and temporal patterns used in exposures.

has substantially greater PTS, than either the "Burst" or "One per second" groups. Apossible reason for the greater PTS suffered by the "Salvo" group is that the first impulse in the pair causes a temporary condition of vulnerability in the cochlea and the second im- pulse caused greater than normal damage because of the increased susceptibility to damage from the sec- ond impulse in the pair. The "Period of vulnerability" may be quite short (less than 1 s), because, for the same acoustic energy, the "Salvo" condition produces more hearing loss than the "One per second" condi- tion.

The data for the lower level (135 dB peak SPL) exposures are shown in the bottom two panels of Fig. 6. The "Burst" condition suffered much less TTS than the other two conditions (p < 0.07), and no PTS was generated among any of the 135 dB groups. Apparently, the damage from the lower levels of impulses was less traumatizing and caused less ro- bust changes in hearing sensitivity than did the higher levels of impulses. The audiometric data at fifteen minutes after the exposure and at 30 days (PTS) have been replotted in Fig. 7 to facilitate more direct comparison between the effects of the high and low exposures. The differences between the 135 and 150 dB exposures were not that great immediately after the exposure, but the 150 dB exposure did pro- duce, on the average, 8 to 22 dB more PTS than the 135 exposure (p < 0.0163).

These data have implications for several debated issues concerning noise-induced hearing loss. First, all these exposures have the same total energy, thus

any of the energy-related theories (Ward et al. 1983) would predict equal amounts of hearing loss, when in fact there were substantial differences. Second, the low- and high-burst conditions produced much less TTS and PTS than the other conditions. Thus the acoustic reflex may play a role in protecting the ear even for high frequency impulses. Third, the high level "Salvo" may have caused more PTS because the first impulse may have "primed" the cochlea for dam- age by the second impulse in the pair. The primary effects appear to be short lived, because the "One per second" group developed substantially less hearing loss. Finally, the higher level "Salvo" and "One per second" produced significantly more PTS than the respective lower-level conditions. It may be hypoth- esized that the high-level conditions exceed the crit- ical level, and were more damaging because they had a direct mechanical effect on the cochlea. Unfortu- nately none of the cochleas was examined imme- diately after the exposure so direct comparisons to the results of Hamernik et al. (1984) were not possi- ble.

C O N C L U S I O N

Noise-induced hearing loss was studied with both impact and impulse noise. For both noise signatures, the effects are not predicted by a simple energy hy- pothesis. The relation between peak amplitude and hearing loss is complicated, suggesting that for each waveform there is a critical level (i.e., be- tween 119 and 125 dB for the impact and between 135 and 150 dB for the impulse). Finally, the actual

Critical level and impact noise 361

transition across the critical level is partially depen- dent on the rate of presentation or the temporal pat- tern.

A c k n o w l e d g m e n t ~ This research was supported by a grant from the National Institute of Occupational Safety and Health.

REFERENCES

Atherley, C.R.C. Noise-induced hearing loss: the energy principle for recurrent impact noise and noise exposure close to the recommended limits. Ann. Occup. Hyg. 16:183; 1973.

Blakeslee, E.A.; Hynson, K.; Hamernik, and Henderson, D. Asymptotic threshold shift in chinchillas exposed to impulse noise. J. Acoust. Soc. Am. 63:876; 1978.

Borg, E.; Nilsson, R. Acoustic reflex in industrial noise. In: Silman, S., ed. The acoustic reflex. New York: Academic Press; 1984.

Burns, W.; Robinson, D.W. Hearing and noise in industry. London, England: Her Majesty's Stationery Office; 1970.

Burns, W.; Robinson, D.W. The concept of noise pollution level. National Physical Lab, Aerodynamics Div. MPL Aero Report AC 38; 1969.

Hamernik, R.P.; Turrentine, G.; Roberto, M.; Salvi, R.J.; Hender- son, D. Anatomical correlates of impulse noise-induced me- chanical damage in the cochlea. Hearing Res. 13:229; 1984a.

Hamernik, R.; Turrentine, G.; Wright, C. G. Surface morphology of the inner sulcus and related epithelial cells of the cochlea following acoustic trauma. Hearing Res. 16:143; 1984b.

Henderson, D.; Hamernik, R.P.; Woodward, C.; Sider, R.W.; Salvi, R.J. Evoked-response audibility curve of the chinchillas. J. Acoust. Soc. Am. 54:1099; 1973.

Henderson, D.; Hamernik, R.P. Asymptotic threshold shift from impulse noise. In: Hamernik, R.P.; Henderson, C.; Salvi, R.J., eds. New perspectives on noise-induced hearing loss. New York: Raven; 1982.

Mills, J.H. Effects of noise on auditory sensitivity, psychophysical tuning curves and suppression. In: New perspectives on noise- induced hearing loss. hamernik, R.P.; Henderson, D.; Salvi, R.J. New York: Raven; 1982.

Passchier-Vermeer, W. Measurement and rating of impulse noise in relation to noise-induced hearing loss. In: Rossi, G., ed. Noise as a public health problem. Proc. fourth international congress. Milano, Italy; 1983.

Perkins, C.; Hamernik, R.P.; Henderson, D. The effect of inter- stimulus interval on the production of hearing loss from im- pulse noise. J. Acoust. Soc. Am. (Suppl. I) 57, $62; 1975.

Price, G. R. Effect of interrupting recovery on loss in cochlear microphonic sensitivity. J. Aconst. Soc. Am. 59(3):709; 1976.

Price, G. R. Impulse noise hazard as a function of level and spectral distribution. In: Saw; Henderson; Hamernik; Colletti, eds. Basic and applied aspects of noise induced hearing loss. New York: Plenum; 1986.

Spoendlin, H.; Brun, J.P. Relation of structural damage to expo- sure time and intensity in acoustic trauma. Acta Otolaryng. 75:220; 1973.

Ward, W.D.; Turner, C.W.; Fabry, D.A. The total energy and equal energy principles in the chinchillas. Rossi, G., ed. Noise as a public health problem. Milano, Italy: Centro Ricerche E Studi Amplifon Kovino; 1983.